Lack of episodic growth hormone secretion in rats with anterolateral deafferentation of the medial-basal hypothalamus

1982 ◽  
Vol 94 (1) ◽  
pp. 77-81 ◽  
Author(s):  
M. Kárteszi ◽  
J. Fiók ◽  
G. B. Makara

Growth hormone secretory dynamics were studied in rats sampled through chronic indwelling right atrial cannulae at time-intervals ranging from 2 days to 2 months after placing an anterolateral cut (ALC) around the medial-basal hypothalamus (MBH). The episodic secretion normally occurring in the control animals could not be seen in the rats with an ALC. Instead of the usual high bursts and low trough levels occurring between 09.00 and 13.00 h in the controls, the operated animals had fairly constant plasma GH levels with only minor fluctuations at all postoperative time-points studied. These results suggest that (1) the isolated MBH is incapable of maintaining the episodic secretion of GH and (2) the pulsatile hormone release is dependent on neural pathways entering the MBH from an anterolateral direction.

1979 ◽  
Vol 91 (3) ◽  
pp. 428-436 ◽  
Author(s):  
Ichiji Wakabayashi ◽  
Megumi Kanda ◽  
Nobuyasu Miki ◽  
Reiko Demura ◽  
Kazuo Shizume

ABSTRACT Effects of chlorpromazine (CPZ) on plasma GH and prolactin levels were observed in conscious rats provided with chronic indwelling right atrial cannulae. The administration of CPZ (200 μg/100 g b.w. iv) suppressed episodic plasma GH burst and resulted in significant elevations of plasma prolactin levels. These were also observed in rats in which two types of hypothalamic deafferentation, i.e. anterior and complete, had been carried out. The data suggest that CPZ acts within the medial basal hypothalamus and inhibits episodic plasma GH secretion. In addition, it is inferred that catecholamines are involved in the generation of episodic plasma GH burst.


1990 ◽  
Vol 126 (2) ◽  
pp. 237-244 ◽  
Author(s):  
R. W. Lea ◽  
C. A. Ahene ◽  
J. A. Marsh ◽  
S. Harvey

ABSTRACT The i.c.v. administration of 0·1 or 10 μg ovine (o)GH to 12- to 16-week-old hypothyroid chickens of a sex-linked dwarf (SLD) strain suppressed the basal plasma GH concentrations, measured 24 h afterwards. The GH response of the oGH-injected SLDs to TRH was suppressed, in a dose-related way, in comparison with that induced by TRH in birds given control injections (10 μg) of bovine serum albumin (BSA). Basal circulating concentrations of GH in euthyroid K strain birds of the same age were even lower than in the SLDs following injection of 10 μg oGH, and were not further reduced by oGH administration. The GH response to TRH in the K strain birds injected i.c.v. with 0·1 or 10 μg oGH was, nevertheless, suppressed in comparison with the BSA-injected K strain controls. The i.c.v. administration of oGH also suppressed circulating concentrations of LH and the LH response to TRH in the K strain birds. Twenty-four hours after i.c.v. administration of oGH (10 μg), the somatostatin (SRIF) content in the medial basal hypothalamus of 8-week-old euthyroid cockerels was greater than that in BSA (10 μg)-injected controls. At the same time, the binding of [3H]3-methyl-histidine2-TRH to the pituitary caudal and cephalic lobes of GH-injected birds was less than that in the controls. These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release. Journal of Endocrinology (1990) 126, 237–244


1987 ◽  
Vol 253 (4) ◽  
pp. E354-E359
Author(s):  
K. Ishikawa ◽  
H. Katakami ◽  
L. A. Frohman

The inhibitory effect of centrally administered thyrotropin-releasing hormone (TRH) on the plasma growth hormone (GH) response to GH-releasing hormone (GHRH) in the rat was studied in relation to the anatomic loci involved. Experiments were performed in animals with bilateral electrolytic lesions in the medial preoptic (MPO) area or with anterolateral hypothalamic deafferentation and in sham-operated controls. Blood samples were obtained every 10 to 20 min from and drugs were injected into freely moving animals with indwelling cannulas in the right atrium and lateral cerebral ventricle. In control animals, the plasma GH response to GHRH, 1 microgram iv, was almost completely inhibited by TRH, 1 microgram icv, injected 5 min previously. In animals with either MPO lesions or anterolateral hypothalamic deafferentation in which median eminence somatostatin immunochemical staining was almost completely eliminated, the GH response to GHRH was enhanced and TRH did not exhibit any inhibitory effect. These results, together with the previous observation that the inhibitory effect of TRH is blocked by prior treatment with anti-somatostatin serum, suggest that the effect of TRH is mediated by stimulation of somatostatin-containing neurons in the periventricular nucleus of the MPO area.


1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


Diabetes ◽  
1975 ◽  
Vol 24 (9) ◽  
pp. 842-850 ◽  
Author(s):  
D. Bryce ◽  
M. Yeh ◽  
C. Funderburk ◽  
H. Todd ◽  
F. Hertelendy

1982 ◽  
Vol 69 (1) ◽  
pp. 104-112 ◽  
Author(s):  
L. Cass Terry ◽  
W. R. Crowley ◽  
M. D. Johnson

Author(s):  
R. Collu ◽  
G. Charpenet ◽  
M. J. Clermont

SUMMARY:The intraperitoneal (IP) or intraventricular (IVT) administration of small amounts of taurine did not modify pentobarbital-induced sleep or pituitary hormone release. However, the drastic increment in plasma GH values induced by morphine administration was completely blocked by the IVT injection of the amino acid. Whether taurine plays a physiological role in the control ofGH secretion is highly speculative.


1982 ◽  
Vol 35 (1) ◽  
pp. 43-47 ◽  
Author(s):  
C. Netti ◽  
F. Guidobono ◽  
V.R. Olgiati ◽  
V. Sibilia ◽  
F. Pagani ◽  
...  

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